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Possible Involvement of Endothelin Peptides and L-Arginine-Nitric Oxide Pathway on the Effect of Endotoxin in the Rabbit Isolated Perfused Kidney

机译:内皮素肽和左旋精氨酸的可能参与 氧化途径对内毒素对家兔离体肾脏的影响

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摘要

Escherichia coli endotoxin (LPS) when infused through the renalartery of the rabbit isolated perfused kidney prepared as constantpressure mode, caused a decrease in flow rate and kidney weightindicating its primary vasoconstrictor effect. This effect waspredominant in kidneys from rabbits pretreated with LPS. Endothelin-1at a concentration of 10−10 M and big endothelin-1 at a concentrationof 10−8 M produced equal vasoconstrictor effects in kidney. Additionof endotheHn converting enzyme inhibitor, phosphoramidon, to theperfusion medium at a concentration of 10−6 M caused a reduction inthe effects of both LPS and big ET-1 without altering thevasoconstrictor effect of ETol. However, addition of methylene blue(10−5 M), a soluble guanylate cyclase inhibitor andNG-nitro-L-arginine-methyl ester (10−6 M) to the perfusion mediumcaused a potentiation in the vasoconstrictor effect of LPS.Indomethacin at a concentration of 10−6 M did not alter the effect ofLPS. These results were taken as evidence for the participation ofendothelin peptides and the L-arginine-nitric oxide pathway in theeffect ofLPS in rabbit isolated perfused kidney.
机译:大肠杆菌内毒素(LPS)通过恒压方式制备的兔离体灌注肾脏的肾动脉注入时,导致流速降低和肾脏重量下降,表明其主要的血管收缩作用。在用LPS预处理的兔子的肾脏中,这种作用最为明显。浓度为10-10 M的内皮素-1和浓度为10-8 M的大内皮素-1在肾脏中产生相同的血管收缩作用。在灌注培养基中以10-6 M的浓度添加内皮素转化酶抑制剂磷酰胺,可降低LPS和大ET-1的作用,而不会改变ETol的血管收缩作用。但是,向灌注培养基中添加亚甲基蓝(10-5 M),可溶性鸟苷酸环化酶抑制剂和NG-硝基-L-精氨酸甲酯(10-6 M)会增强LPS的血管收缩作用。 10-6 M的浓度不会改变LPS的作用。这些结果被认为是内皮素肽和L-精氨酸一氧化氮途径参与家兔离体肾脏灌注的LPS效应的证据。

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